Comparison of the effects of [Phe1Ψ(CH2‐NH)Gly2]Nociceptin (1–13)NH2 in rat brain, rat vas deferens and CHO cells expressing recombinant human nociceptin receptors
Nociceptin(NC) is the endogenous ligand for the opioid receptor like‐1 receptor (NC‐receptor). [Phe1ΨC(CH2‐NH)Gly2]Nociceptin(1–13)NH2 ([F/G]NC(1–13)NH2) has been reported to antagonize NC actions in peripheral guinea‐pig and mouse tissues. In this study, we investigated the effects of a range of NC...
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| Veröffentlicht in: | British journal of pharmacology 1999-05, Vol.127 (1), p.123-130 |
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| creator | Okawa, Hirobumi Nicol, Beverley Bigoni, Raffaella Hirst, Robert A Calo', Girolamo Guerrini, Remo Rowbotham, David J Smart, Darren McKnight, Alexander T Lambert, David G |
| description | Nociceptin(NC) is the endogenous ligand for the opioid receptor like‐1 receptor (NC‐receptor). [Phe1ΨC(CH2‐NH)Gly2]Nociceptin(1–13)NH2 ([F/G]NC(1–13)NH2) has been reported to antagonize NC actions in peripheral guinea‐pig and mouse tissues. In this study, we investigated the effects of a range of NC C‐terminal truncated fragments and [F/G]NC(1–13)NH2 on NC receptor binding, glutamate release from rat cerebrocortical slices (rCX), inhibition of cyclic AMP accumulation in CHO cells expressing the NC receptor (CHONCR) and electrically evoked contractions of the rat vas deferens (rVD).
In radioligand binding assays, a range of ligands inhibited [125I]‐Tyr14‐NC binding in membranes from rCX and CHONCR cells. As the peptide was truncated there was a general decline in pKi. [F/G]NC(1–13)NH2 was as potent as NC(1–13)NH2.
The order of potency for NC fragments to inhibit cyclic AMP accumulation in whole CHONCR cells was NCNH2NC=NC(1–13)NH2>NC(1–12)NH2>>NC(1–11)NH2. [F/G]NC(1–13)NH2 was a full agonist with a pEC50 value of 8.65.
NCNH2 and [F/G]NC(1–13)NH2 both inhibited K+ evoked glutamate release from rCX with pEC50 and maximum inhibition of 8.16, 48.5±4.9% and 7.39, 58.9±6.8% respectively.
In rVD NC inhibited electrically evoked contractions with a pEC50 of 6.63. Although [F/G]NC(1–13)NH2, displayed a small (instrinsic activity α=0.19) but consistent residual agonist activity, it acted as a competitive antagonist (pA2 6.76) in the rVD.
The differences between [F/G]NC(1–13)NH2 action on central and peripheral NC signalling could be explained if [F/G]NC(1–13)NH2 was a partial agonist with high strength of coupling in the CNS and low in the periphery. An alternative explanation could be the existence of central and peripheral receptor isoforms.
British Journal of Pharmacology (1999) 127, 123–130; doi:10.1038/sj.bjp.0702539 |
| doi_str_mv | 10.1038/sj.bjp.0702539 |
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In radioligand binding assays, a range of ligands inhibited [125I]‐Tyr14‐NC binding in membranes from rCX and CHONCR cells. As the peptide was truncated there was a general decline in pKi. [F/G]NC(1–13)NH2 was as potent as NC(1–13)NH2.
The order of potency for NC fragments to inhibit cyclic AMP accumulation in whole CHONCR cells was NCNH2NC=NC(1–13)NH2>NC(1–12)NH2>>NC(1–11)NH2. [F/G]NC(1–13)NH2 was a full agonist with a pEC50 value of 8.65.
NCNH2 and [F/G]NC(1–13)NH2 both inhibited K+ evoked glutamate release from rCX with pEC50 and maximum inhibition of 8.16, 48.5±4.9% and 7.39, 58.9±6.8% respectively.
In rVD NC inhibited electrically evoked contractions with a pEC50 of 6.63. Although [F/G]NC(1–13)NH2, displayed a small (instrinsic activity α=0.19) but consistent residual agonist activity, it acted as a competitive antagonist (pA2 6.76) in the rVD.
The differences between [F/G]NC(1–13)NH2 action on central and peripheral NC signalling could be explained if [F/G]NC(1–13)NH2 was a partial agonist with high strength of coupling in the CNS and low in the periphery. An alternative explanation could be the existence of central and peripheral receptor isoforms.
British Journal of Pharmacology (1999) 127, 123–130; doi:10.1038/sj.bjp.0702539</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0702539</identifier><identifier>PMID: 10369464</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; binding ; Binding, Competitive ; Biological and medical sciences ; Cerebral Cortex - drug effects ; Cerebral Cortex - metabolism ; CHO Cells ; Cricetinae ; cyclic AMP ; Cyclic AMP - metabolism ; Electric Stimulation ; Female ; glutamate release ; Glutamic Acid - metabolism ; Humans ; In Vitro Techniques ; Ligands ; Male ; Medical sciences ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - physiology ; Neuropharmacology ; Neurotransmitters. Neurotransmission. Receptors ; nociceptin receptor ; Nociceptin/orphanin FQ ; Opioid Peptides - pharmacology ; Peptide Fragments - pharmacology ; Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems ; Pharmacology. Drug treatments ; rat ; Rats ; Rats, Wistar ; Receptors, Opioid - biosynthesis ; Recombinant Proteins - biosynthesis ; vas deferens ; Vas Deferens - drug effects ; Vas Deferens - metabolism ; Vas Deferens - physiology</subject><ispartof>British journal of pharmacology, 1999-05, Vol.127 (1), p.123-130</ispartof><rights>1999 Nature Publishing Group</rights><rights>1999 INIST-CNRS</rights><rights>Copyright 1999, Nature Publishing Group 1999 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566005/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566005/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,724,777,781,882,1412,1428,27905,27906,45555,45556,46390,46814,53772,53774</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1781445$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10369464$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Okawa, Hirobumi</creatorcontrib><creatorcontrib>Nicol, Beverley</creatorcontrib><creatorcontrib>Bigoni, Raffaella</creatorcontrib><creatorcontrib>Hirst, Robert A</creatorcontrib><creatorcontrib>Calo', Girolamo</creatorcontrib><creatorcontrib>Guerrini, Remo</creatorcontrib><creatorcontrib>Rowbotham, David J</creatorcontrib><creatorcontrib>Smart, Darren</creatorcontrib><creatorcontrib>McKnight, Alexander T</creatorcontrib><creatorcontrib>Lambert, David G</creatorcontrib><title>Comparison of the effects of [Phe1Ψ(CH2‐NH)Gly2]Nociceptin (1–13)NH2 in rat brain, rat vas deferens and CHO cells expressing recombinant human nociceptin receptors</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Nociceptin(NC) is the endogenous ligand for the opioid receptor like‐1 receptor (NC‐receptor). [Phe1ΨC(CH2‐NH)Gly2]Nociceptin(1–13)NH2 ([F/G]NC(1–13)NH2) has been reported to antagonize NC actions in peripheral guinea‐pig and mouse tissues. In this study, we investigated the effects of a range of NC C‐terminal truncated fragments and [F/G]NC(1–13)NH2 on NC receptor binding, glutamate release from rat cerebrocortical slices (rCX), inhibition of cyclic AMP accumulation in CHO cells expressing the NC receptor (CHONCR) and electrically evoked contractions of the rat vas deferens (rVD).
In radioligand binding assays, a range of ligands inhibited [125I]‐Tyr14‐NC binding in membranes from rCX and CHONCR cells. As the peptide was truncated there was a general decline in pKi. [F/G]NC(1–13)NH2 was as potent as NC(1–13)NH2.
The order of potency for NC fragments to inhibit cyclic AMP accumulation in whole CHONCR cells was NCNH2NC=NC(1–13)NH2>NC(1–12)NH2>>NC(1–11)NH2. [F/G]NC(1–13)NH2 was a full agonist with a pEC50 value of 8.65.
NCNH2 and [F/G]NC(1–13)NH2 both inhibited K+ evoked glutamate release from rCX with pEC50 and maximum inhibition of 8.16, 48.5±4.9% and 7.39, 58.9±6.8% respectively.
In rVD NC inhibited electrically evoked contractions with a pEC50 of 6.63. Although [F/G]NC(1–13)NH2, displayed a small (instrinsic activity α=0.19) but consistent residual agonist activity, it acted as a competitive antagonist (pA2 6.76) in the rVD.
The differences between [F/G]NC(1–13)NH2 action on central and peripheral NC signalling could be explained if [F/G]NC(1–13)NH2 was a partial agonist with high strength of coupling in the CNS and low in the periphery. An alternative explanation could be the existence of central and peripheral receptor isoforms.
British Journal of Pharmacology (1999) 127, 123–130; doi:10.1038/sj.bjp.0702539</description><subject>Animals</subject><subject>binding</subject><subject>Binding, Competitive</subject><subject>Biological and medical sciences</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cerebral Cortex - metabolism</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>cyclic AMP</subject><subject>Cyclic AMP - metabolism</subject><subject>Electric Stimulation</subject><subject>Female</subject><subject>glutamate release</subject><subject>Glutamic Acid - metabolism</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Ligands</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>Neuropharmacology</subject><subject>Neurotransmitters. Neurotransmission. Receptors</subject><subject>nociceptin receptor</subject><subject>Nociceptin/orphanin FQ</subject><subject>Opioid Peptides - pharmacology</subject><subject>Peptide Fragments - pharmacology</subject><subject>Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems</subject><subject>Pharmacology. Drug treatments</subject><subject>rat</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Opioid - biosynthesis</subject><subject>Recombinant Proteins - biosynthesis</subject><subject>vas deferens</subject><subject>Vas Deferens - drug effects</subject><subject>Vas Deferens - metabolism</subject><subject>Vas Deferens - physiology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVksFu1DAQhiMEokvhyhH5gFArkcWOY8e5IEEETaVq2wOcELIc76TrKLGDnS3srY-AxEv0aXiIPgnedqHlNDP6v_l_WZ4keU7wnGAq3oRu3nTjHBc4Y7R8kMxIXvCUUUEeJjOMcZESIsRe8iSEDuMoFuxxshdXeZnzfJZcVW4YlTfBWeRaNK0AQduCnsJ2_HK2AvL76qCqs-vLn4v68KjfZF8XThsN42QsOiDXl78IPVzUGYqjVxNqvDL29U17oQJaQgsebEDKLlFVnyINfR8Q_Bg9hGDsOfKg3dAYq-yEVutBWWTvAqIYG-fD0-RRq_oAz3Z1P_n88cOnqk5PTo-Oq3cnaZfnhKa6BaoJ5hyIYrxdZrkuCdeYC6HKTDe0UA3jeVsyDbzRutRlhkshGCuaSCi6n7y99R3XzQBLDXbyqpejN4PyG-mUkf8r1qzkubuQhHGOMYsGr3YG3n1bQ5jkYML20cqCWwfJS0EKgWkEX9xP-hfx93Mi8HIHqKBV33pltQl3XCFInm8D6S323fSwuWezdRIydDJeiNxdiHx_VhNCKf0D5e6y-g</recordid><startdate>199905</startdate><enddate>199905</enddate><creator>Okawa, Hirobumi</creator><creator>Nicol, Beverley</creator><creator>Bigoni, Raffaella</creator><creator>Hirst, Robert A</creator><creator>Calo', Girolamo</creator><creator>Guerrini, Remo</creator><creator>Rowbotham, David J</creator><creator>Smart, Darren</creator><creator>McKnight, Alexander T</creator><creator>Lambert, David G</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>199905</creationdate><title>Comparison of the effects of [Phe1Ψ(CH2‐NH)Gly2]Nociceptin (1–13)NH2 in rat brain, rat vas deferens and CHO cells expressing recombinant human nociceptin receptors</title><author>Okawa, Hirobumi ; Nicol, Beverley ; Bigoni, Raffaella ; Hirst, Robert A ; Calo', Girolamo ; Guerrini, Remo ; Rowbotham, David J ; Smart, Darren ; McKnight, Alexander T ; Lambert, David G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j4413-cfe3c1066e1a56fd24c916c0688a92cb37ab564f95ce6bcc9c920988557b8a9a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>binding</topic><topic>Binding, Competitive</topic><topic>Biological and medical sciences</topic><topic>Cerebral Cortex - drug effects</topic><topic>Cerebral Cortex - metabolism</topic><topic>CHO Cells</topic><topic>Cricetinae</topic><topic>cyclic AMP</topic><topic>Cyclic AMP - metabolism</topic><topic>Electric Stimulation</topic><topic>Female</topic><topic>glutamate release</topic><topic>Glutamic Acid - metabolism</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Ligands</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Neuropharmacology</topic><topic>Neurotransmitters. Neurotransmission. Receptors</topic><topic>nociceptin receptor</topic><topic>Nociceptin/orphanin FQ</topic><topic>Opioid Peptides - pharmacology</topic><topic>Peptide Fragments - pharmacology</topic><topic>Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems</topic><topic>Pharmacology. Drug treatments</topic><topic>rat</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Opioid - biosynthesis</topic><topic>Recombinant Proteins - biosynthesis</topic><topic>vas deferens</topic><topic>Vas Deferens - drug effects</topic><topic>Vas Deferens - metabolism</topic><topic>Vas Deferens - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Okawa, Hirobumi</creatorcontrib><creatorcontrib>Nicol, Beverley</creatorcontrib><creatorcontrib>Bigoni, Raffaella</creatorcontrib><creatorcontrib>Hirst, Robert A</creatorcontrib><creatorcontrib>Calo', Girolamo</creatorcontrib><creatorcontrib>Guerrini, Remo</creatorcontrib><creatorcontrib>Rowbotham, David J</creatorcontrib><creatorcontrib>Smart, Darren</creatorcontrib><creatorcontrib>McKnight, Alexander T</creatorcontrib><creatorcontrib>Lambert, David G</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Okawa, Hirobumi</au><au>Nicol, Beverley</au><au>Bigoni, Raffaella</au><au>Hirst, Robert A</au><au>Calo', Girolamo</au><au>Guerrini, Remo</au><au>Rowbotham, David J</au><au>Smart, Darren</au><au>McKnight, Alexander T</au><au>Lambert, David G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comparison of the effects of [Phe1Ψ(CH2‐NH)Gly2]Nociceptin (1–13)NH2 in rat brain, rat vas deferens and CHO cells expressing recombinant human nociceptin receptors</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1999-05</date><risdate>1999</risdate><volume>127</volume><issue>1</issue><spage>123</spage><epage>130</epage><pages>123-130</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Nociceptin(NC) is the endogenous ligand for the opioid receptor like‐1 receptor (NC‐receptor). [Phe1ΨC(CH2‐NH)Gly2]Nociceptin(1–13)NH2 ([F/G]NC(1–13)NH2) has been reported to antagonize NC actions in peripheral guinea‐pig and mouse tissues. In this study, we investigated the effects of a range of NC C‐terminal truncated fragments and [F/G]NC(1–13)NH2 on NC receptor binding, glutamate release from rat cerebrocortical slices (rCX), inhibition of cyclic AMP accumulation in CHO cells expressing the NC receptor (CHONCR) and electrically evoked contractions of the rat vas deferens (rVD).
In radioligand binding assays, a range of ligands inhibited [125I]‐Tyr14‐NC binding in membranes from rCX and CHONCR cells. As the peptide was truncated there was a general decline in pKi. [F/G]NC(1–13)NH2 was as potent as NC(1–13)NH2.
The order of potency for NC fragments to inhibit cyclic AMP accumulation in whole CHONCR cells was NCNH2NC=NC(1–13)NH2>NC(1–12)NH2>>NC(1–11)NH2. [F/G]NC(1–13)NH2 was a full agonist with a pEC50 value of 8.65.
NCNH2 and [F/G]NC(1–13)NH2 both inhibited K+ evoked glutamate release from rCX with pEC50 and maximum inhibition of 8.16, 48.5±4.9% and 7.39, 58.9±6.8% respectively.
In rVD NC inhibited electrically evoked contractions with a pEC50 of 6.63. Although [F/G]NC(1–13)NH2, displayed a small (instrinsic activity α=0.19) but consistent residual agonist activity, it acted as a competitive antagonist (pA2 6.76) in the rVD.
The differences between [F/G]NC(1–13)NH2 action on central and peripheral NC signalling could be explained if [F/G]NC(1–13)NH2 was a partial agonist with high strength of coupling in the CNS and low in the periphery. An alternative explanation could be the existence of central and peripheral receptor isoforms.
British Journal of Pharmacology (1999) 127, 123–130; doi:10.1038/sj.bjp.0702539</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10369464</pmid><doi>10.1038/sj.bjp.0702539</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals binding Binding, Competitive Biological and medical sciences Cerebral Cortex - drug effects Cerebral Cortex - metabolism CHO Cells Cricetinae cyclic AMP Cyclic AMP - metabolism Electric Stimulation Female glutamate release Glutamic Acid - metabolism Humans In Vitro Techniques Ligands Male Medical sciences Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - physiology Neuropharmacology Neurotransmitters. Neurotransmission. Receptors nociceptin receptor Nociceptin/orphanin FQ Opioid Peptides - pharmacology Peptide Fragments - pharmacology Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems Pharmacology. Drug treatments rat Rats Rats, Wistar Receptors, Opioid - biosynthesis Recombinant Proteins - biosynthesis vas deferens Vas Deferens - drug effects Vas Deferens - metabolism Vas Deferens - physiology |
| title | Comparison of the effects of [Phe1Ψ(CH2‐NH)Gly2]Nociceptin (1–13)NH2 in rat brain, rat vas deferens and CHO cells expressing recombinant human nociceptin receptors |
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